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1.
Figure 3

Figure 3. Electron Microscopy Findings in the Renal Biopsy. From: Novel X-linked glomerulopathy associated with a COL4A5 missense mutation in a noncollagenous interruption.

Electron microscopy results are presented with electron dense immune complex (arrows) deposition. Effacement of the podocyte foot processes is present (arrowheads).

Brian Becknell, et al. Kidney Int. ;79(1):120-127.

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2.
Figure 1

Figure 1. Extended Pedigree. From: Novel X-linked glomerulopathy associated with a COL4A5 missense mutation in a noncollagenous interruption.

Carriers are indicated by gray circles. Affected males are indicated by black squares. Individual 308 (square with vertical stripes) died of renal failure by history; however records to determine the precise etiology were not available. The index patient is indicated by an arrow.

Brian Becknell, et al. Kidney Int. ;79(1):120-127.

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3.
Figure 5

Figure 5. Phylogenetic Conservation of the Phe 222 Residue. From: Novel X-linked glomerulopathy associated with a COL4A5 missense mutation in a noncollagenous interruption.

Type 4 collagens consist of a minor noncollagenous domain, a minor collagenous (7S) domain, a major collagenous domain containing 15–20 noncollagenous interruptions and a carboxyl terminal noncollagenous (NC1) domain, . The area of the noncollagenous interruption affected by the p.F222C mutation is represented by the dashed lines. The alignment of the predicted COL4A5 protein sequences from twelve species reveals the complete conservation of Phe222 residue in vertebrates.

Brian Becknell, et al. Kidney Int. ;79(1):120-127.

CitationFull text

4.
Figure 4

Figure 4. Renal Survival Curves. From: Novel X-linked glomerulopathy associated with a COL4A5 missense mutation in a noncollagenous interruption.

Patients with the p.F222C mutation (n = 7) progressed to ESRD at a more rapid rate than historical controls with splice site mutations (n = 13), missense mutations (n = 21) and large rearrangements, nonsense and deletion/insertion mutations (n = 23) reported by Martin et al and Gross et al. Differences between patients with the p.F222C mutation and patients with other types of mutations were highly significant (P < 0 .001).

Brian Becknell, et al. Kidney Int. ;79(1):120-127.

CitationFull text

5.
Figure 2

Figure 2. Light Microscopy and Immunohistochemistry Findings in the Renal Biopsy. From: Novel X-linked glomerulopathy associated with a COL4A5 missense mutation in a noncollagenous interruption.

Jones silver staining (left panel) demonstrated segmental sclerosis (arrows). No splitting, spikes or lucencies were evident in the GBM (arrowheads) PAS staining (right panel) demonstrates mesangioproliferative glomerulonephritis with increased mesangial matrix and mesangial cellularity (arrowheads). Magnification 400×. (B) Staining for α1(IV), α3(IV) and α5(IV) collagen was found in the GBM (arrowheads), although α3(IV) staining was slightly diminished in affecteds. Positive staining was present in the tubular basement membranes (arrows); this staining was diffuse for α1(IV) collagen and focal for α3 (not shown) and α5 chains of type IV collagen. α1(IV) and α5(IV) collagen was also expressed in the basement membranes of Bowman's capsule (asterisks).

Brian Becknell, et al. Kidney Int. ;79(1):120-127.

CitationFull text

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